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Bact/fungal path
Lecture11-12
| Question | Answer |
|---|---|
| outcomes of encounter between microorganism and host | infection and damageestablishment of a permanent relationshipinapparent/subclinical infectionprevention of infection or complete clearance |
| what influences the outcome | microorganism's ability to breah host barriers and evade destructiontactics for replication, spread, establishment of infection, and causation of diseaseinnate and adaptive immunologic abilityability to transmit itself to a new susceptible host |
| stages in a pathogenic process | exposure and entryattachmentinvasioneffects on the hostevasion of immune responsesdissemination |
| attachment | adhesion=physical attachment to a cell or surfacebacteria can adhere to internal, external, or artificial surfacesnecessary first step in order to permanently colonize |
| factors that influence colonization | ability to adherefavorable environmentpresence/absence of normal microflora/commensals |
| receptors for attachment | can be specialized protein, component of a cellular membrane, surface component, or a general surface receptor |
| adhesins | 1. Pili and finbriae: expressin may be coordinated with other virulence factors2. Afimbrial adhesions: ligands can be any cell structure |
| invasion | not all bacteria have to enter host cells to replicatephagocytitic cells: enter by phagocytosisnon phagocytitic cells: many ways |
| invasins | bacterial surface proteins that interact with specific receptors to induce endocytosis |
| host cell cytoskeleton rearrangement | triggered by injection of bacterial proteins into host cell leading to membrane ruffling |
| Why are some infections inapparent/subacute? | infected tissue is undamagedinfection is controlled before organism reaches its target tissuetarget tissue is expendable or rapidly repairedextent of damage is below a functional threshold |
| chronic/persistent infection | microorganism continually detectable at low levelsmay have mild or no clinical symptoms (Typhoid fever) |
| latent infection | virus not continually detectableintermittent reactivation leads to microorganism detectable/shed again (TB) |
| immunopathology | damage to host cells as a result of the microbally induced immune response |
| direct damage | cytolytic effecttoxinsphysical growthtoxic structuresdegradative enzymes |
| degradative enzymes | produced by tissue damaging pathogensimportant in establishing spread, release of growth substrates1. hyaluronidase (breaks down hyaluronic acid of connective tissue)2. streptokinase (breaks down fibrin clots)3. collaginase (breaks down collagen) |
| toxic structures | gram- LPSmultiple, concentration dependent effects |
| physical growth | growth of hyphae push through cell walls and damage tissues |
| toxins | exotoxinssecreted into extracellular environmentvery potent at low concentrationsgram + and - |
| Exotoxins | toxic in small amountsspecific effectspolypeptidestoxoid formationno fever stimulationsecreted from live cellsgram+ and - |
| endotoxins | toxic is high dosessystemic effects, fever, inflammationLPS in cell wallno toxoid formationcell lysis as releasegram- bacteria |
| benefits to the bacteria of exotoxin production | diptheria: colonization of throat by killing polymorphs and epithelial cellscholera: resulting diarrhea aids in transmissionpneumolysin: interfers with host defenses |
| Class I exotoxin | surface acting |
| Class II exotoxins | membrane acting |
| Class III exotoxins | intracellularA: catalytic (Active) domainenzymatically attacks a particular host cell function or structureB: Binding subunitlinked to A by disulfide bondspecific host cell glycoprotein or glycolipid |
| entry of exotoxin | 1. binding to specific receptor on target cell2. entry via RMA or via pores3. internalization--> specific activity at defined target site |
| ADP ribosylation | addition of ADP ribosyl group onto functional cell protein--> change in function/activation of the target proteinex. diptheria toxin: expression triggered by low levels of iron, target: EF-2 |
| Pore formation | channel forming toxins (class II exotoxin)has many targetscell death occurs due to osmotic lysis or apoptosisprotein pores destabilize cell membrane |
| phospholipid membrane destabilization | class II exotoxinsindiscriminate lysisdestabilize cell membrane by removing polar head group from phospholipids |
| zinc metalloprotease | proteolytic cleavage of toxin-->2 linked fragments1. Light chain-enzymatically active2. Heavy chain-binding and translocation |
| Tetanus toxin | produced by clostridium tetanitargets inhibitory interneurons in CNSlight chain targets membrane component of synaptic vessicleinhibition of inhibitory neurotransmittersleads to spastic paralysis |
| Botulinum toxin | produced by clostridium botulinumtargets presynaptic motor neurons (PNS)light chains target membrane component of synaptic vesiclesinhibition of ACh releaseflaccid paralysis |
| toxin based vaccines | toxoid=inactivated exotoxinstill antigenic, but cannot cause damagediptheria/tetanus (examples) |
| pathogenicity islands | clusters of genes encoding for virulence factors such as:toxinssuperantigensiron uptake system/siderophoresadhesinspresent in pathogens but missing in same non-pathogenic speciesassociated with mobile genetic elements |
| coordination of virulence gene response | two component signal transduction systemcoordinate bacterial responses to environmental stimulisensor in cytoplasmic membrane, response regulator in cytoplasm |
| how bacteria obtain iron | synthesis of surface receptors that can grab the host's iron chelatorssynthesis and secretion of siderophores (low molecular weight and high affinityfor iron) |
| evasion of complement | capsules, complement binding proteins, proteases, host cell mimicry |
| evasion of phagocytic killing | capsules, type III secretions, intracellular parasitism |
| evasion of antigen processing | interfere with MHC function and antigen processing |
| evasion of antibodies | Ig-binding/inactivating proteins, antigenic variation |
| evasion of apoptosis | decoy proteins |
| capsule composition | polysaccharide, polyribose ribitol phosphate, hyaluronic acid (host cell mimicry) |
| toxins to kill macrophages and leukocytes | leukocidins-->kill neutrophils and macrophagesalters phospholipid metabolism by ADP ribosylation of a protein controlling phosphotidylinositol-->disruption of cellular activitiesproduced by highly invasive bacteria |
| phagocytic killing | solution: replicate in phagocytic cellsprevent fusion of phagosome & lysosome (legionella)escape into cytosol (L. monocytogenes)resist lysosomal enzymes (histoplasma)inavtivate harmful O2 species (s.aureus) |
| Ig-binding/inactivating proteins | bacterial IgA proteases inactivate sIgA by proteolysisdirect binding of bacteral cell wall protein to Fc domain of IgG |
| Antigenic/phase variation | antigenic variation=multiple antigenic forms can be expressed at different timesphase variation=can switch protein expression on and off |
| biofilm formation | bacterial and/or fingal attachment to a tissue/artificial surface and production of a covering layer of EPS |
| dissemination | enables movement to another site within the body |
| direct movement | surface fluids, flow of intestinal contents, facilitated by toxin production, growth through tissues |
| via nerves | not generally used by bacteria or fungi |
| CSF | cross blood CSF junction, requires movement into bloodstream first |
| Blood | in blood or blood components |
| lymphatics | from tissue fluids into lymphatic capillaries |
| transmission | route by which microorganisms are transfered from a reservoir to a new host |
| transmissibility | number and period of time organisms are shed for |
| routes of transmission | vertical, direct, droplet, fecal oral, sexual, environmental, vector borne |
Created by:
kamarsh
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